This case report presents a 15-year-old female who exhibited paroxysmal episodes of migraine-type headache associated with non-painful manifestations such as motor weakness and visual, sensory, and language aura, illustrating a typical case of hemiplegic migraine. This genetic disorder primarily affects the functioning of ion channels (calcium, sodium, and/or potassium), resulting in either gain (increased glutamate release and seizures) or loss-of-function (promoting cortical spreading depression) consequences, leading to motor and cognitive dysfunction. These alterations are inherited in an autosomal dominant manner; however, sporadic cases are also common. Three genes are known to be involved in the genesis of the disease: CACNA1A (Familial Hemiplegic Migraine Type 1 [FHM1]), ATP1A2 (FHM2), and SNC1A (FHM3). The diagnosis is clinical, epidemiological, and mainly genetic. The attending physician must rule out vascular, infectious, or other genetic causes. Prophylactic treatment is challenging, and acute management is essential to avoid sequelae or fatal outcomes. The main complications include refractory seizures, cognitive decline with progression to deep coma, and strokes secondary to vasospasms.

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Hemiplegic Migraine

  • Elcio Juliato Piovesan,
  • Marco Antonio Takashi Utiumi

摘要

This case report presents a 15-year-old female who exhibited paroxysmal episodes of migraine-type headache associated with non-painful manifestations such as motor weakness and visual, sensory, and language aura, illustrating a typical case of hemiplegic migraine. This genetic disorder primarily affects the functioning of ion channels (calcium, sodium, and/or potassium), resulting in either gain (increased glutamate release and seizures) or loss-of-function (promoting cortical spreading depression) consequences, leading to motor and cognitive dysfunction. These alterations are inherited in an autosomal dominant manner; however, sporadic cases are also common. Three genes are known to be involved in the genesis of the disease: CACNA1A (Familial Hemiplegic Migraine Type 1 [FHM1]), ATP1A2 (FHM2), and SNC1A (FHM3). The diagnosis is clinical, epidemiological, and mainly genetic. The attending physician must rule out vascular, infectious, or other genetic causes. Prophylactic treatment is challenging, and acute management is essential to avoid sequelae or fatal outcomes. The main complications include refractory seizures, cognitive decline with progression to deep coma, and strokes secondary to vasospasms.